Abstract
Previously, we reported significant life-shortening due to early neoplastic death in specific-pathogen-free B6C3F1 mice irradiated with continuous low dose-rate (20 mGy/22 h/day) gamma-irradiation accumulating to a high dose (8000 mGy). To understand the mechanisms of the life-shortening, we transplanted syngeneic tumor cells into both irradiated mice and age-matched, non-irradiated control mice to compare the transplantability of tumor cells. As a result, we found enhanced transplantabilities of tumor cells in irradiated mice. In this report, to understand the mechanisms of the enhanced tumor transplantability, we examined some factors relevant to tumor immunity of irradiated mice.
Since chemokine network was known to be involved in tumor immunity, we focused on combinations of chemokine ligands and chemokine receptors. Using RT-PCR and ELISA, we found that the transplanted tumor cells expressed some chemokine ligands, Ccl2, Ccl5, Ccl25, Cxcl16, and Cx3cl1. These ligands were known to bind to chemokine receptors, Ccr2, Ccr5, Ccr9, Cxcr6, and Cx3cr1, respectively. We analysed expression patterns of 19 chemokine receptors by RT-PCR in both irradiated mice and non-irradiated control mice. Expressions of Ccr5, Ccr9 and Cxcr6 were reduced significantly in irradiated mice.
These results indicated that the expressions of chemokine receptors against chemokine ligands expressed by tumor cells were reduced significantly in mice irradiated with low dose-rate gamma-ray continuously. The relevance of chemokine network to enhanced tumor transplantability in irradiated mice is needed to be investigated in detail. This study was performed under contract with the Aomori Prefectural Government, Japan.
